相互作用するアミノ酸の置換により,毒カエルはエピバティジンに対する耐性を進化させる
Rebecca D Tarvin1, Cecilia M Borghese2, Wiebke Sachs2,3
1Department of Integrative Biology, University of Texas at Austin, Austin, TX 78712, USA. rdtarvin@gmail.com.
Science (New York, N.Y.)
|September 23, 2017
まとめ
毒カエルはニコチンアセチルコリン受容体 (nAChRs) を変えて,自身の毒性エピバチジンに対する耐性を進化させた. この適応は受容体の機能を維持し 動物の化学的防御の進化を示した.
科学分野:
- 進化生物学
- 神経科学
- 生物化学
背景:
- 毒素を産生する動物は 自己中毒のリスクがあり 進化した抵抗メカニズムが必要です
- 毒カエルはエピバティジンのような強力なアルカロイドを使用します ニコチンアセチルコリン受容体 (nAChR) アゴニストは低用量で致死します
- エピバティディンの標的部位とアセチルコレンの重なり合いは,重要な受容体の機能を損なうことなく,抵抗性の進化を困難にします.
研究 の 目的:
- 毒カエルが強力なアルカロイドエピバティジンに 耐性を進化させる 分子機構を調査する
- エピバティジンに対する耐性を与える変異にもかかわらず,nAChRの機能が維持される方法を理解する.
- 毒カエルの化学防御の 進化の経路を解明するためです
主な方法:
- ヒトとカエルのニコチンアセチルコリン受容体 (nAChRs) で電気生理学的測定を行った.
- nAChRにおける特定のアミノ酸置換は,エピバティジンとアセチルコレンの感受性に対する影響を分析した.
- 異なる毒カエルの系統で進化した変異の比較分析.
主要な成果:
- 毒カエルで3回独立して進化した単一のアミノ酸の置換は,エピバチディンの感受性を低下させた.
- この抵抗性変異は アセチルコリンに対する 感受性の低下を伴いました
- その後,系統特有のアミノ酸の変化により,nAChRの機能が回復し,受容体の効率が回復しました.
- これらの発見は,抵抗メカニズムの収束進化を強調しています.
結論:
- 毒カエルは特定のnAChR変異によって 毒素に対する耐性を進化させます
- 抵抗メカニズムの収束的な進化は,本質的な生理学的機能の維持を可能にします.
- nAChRsの遺伝的適応により 毒カエルは高いレベルの 化学的防御を達成できます
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